Paratonia affects 90% to 100% of patients with end-stage dementia, yet it is frequently misdiagnosed.1,2 Paratonia is characterized by involuntary, velocity-dependent resistance to passive movement occurring uniquely in dementia.3 Complications include contractures, pressure ulcers, pain, and caregiver burden.4,5 Traditional pharmacologic treatments are ineffective,6 and forceful passive mobilization may worsen symptoms.5,7 This case demonstrates clinical recognition and evidence-based management strategies of paratonia for family physicians.

The patient is an 86-year-old man with advanced Alzheimer disease (Global Deterioration Scale stage 7)8 who resides in a long-term care facility. Over the past year, staff members observed increasingly marked resistance to passive movement in the patient. His limbs became progressively rigid, especially at the elbows, knees, fingers, and wrists, and he adopted semiflexed postures that interfered considerably with daily care. Maintaining the patient’s personal hygiene became the most distressing issue for caregivers and family—particularly with hand care.

The patient’s involuntary clenched posture of the fingers prevented caregivers from opening his hands to clean the palms. Moisture, skin debris, and food particles accumulated between the digits, leading to recurrent redness, maceration, and malodor, with suspected fungal overgrowth. Nail trimming was almost impossible, increasing the risk of inadvertent injury for both the patient and staff members. During bathing, attempts to clean the patient’s hands elicited visible grimacing, indicating discomfort and pain. Despite diligent care, maintaining satisfactory hygiene for the patient was difficult, raising persistent concerns about dignity, infection risk, and quality of life.

Transferring, dressing, and perineal care for the patient were also hindered by rigidity of larger joints, though hand care was consistently regarded as the greatest challenge. Early pressure areas developed over the patient’s elbows, amplifying the risks associated with immobility. Routine passive mobilization provided minimal relief and occasionally led to increased agitation.

Physical examination of the patient revealed velocity-dependent resistance to passive movement that increased with faster movements and varied with direction, occurring in both flexion and extension. Notably, the resistance was not uniform throughout the range of motion, and there was no clasp-knife phenomenon (the sudden release of resistance characteristic of spasticity). Cogwheeling, which typically accompanies parkinsonian rigidity, was absent. The patient did not exhibit other parkinsonian features such as resting tremor or bradykinesia beyond what would be expected from his advanced dementia.

Because these issues persisted, the patient was referred to a specialty neurology clinic. Following assessment and discussion with the patient’s family, botulinum toxin was administered to focal muscles of his left hand and upper arm. Within 2 weeks, caregivers observed substantial improvement in the patient. His hands could be opened for cleaning and nail trimming, odour resolved, and the patient appeared to experience less discomfort during care.

The clinical benefit of administering botulinum toxin to the muscles of his hand and upper arm lasted about 3 months, after which resistance gradually recurred, and plans for repeat treatment were made.

Paratonia is defined as an involuntary, velocity-dependent, variable resistance to passive movement that occurs uniquely in dementia.3 It differs from spasticity and parkinsonian rigidity, which display distinct velocity and mechanistic features.3 The syndrome can manifest as either facilitatory (involuntary cooperation) or oppositional (active resistance) and typically progresses with disease severity.4 Clinical complications include contractures, pain, pressure ulcers, feeding difficulties, and a meaningful reduction in patient quality of life, with marked physical and psychological burden for caregivers.4,5

Differentiating paratonia from parkinsonian rigidity is clinically important as these conditions may coexist or be confused in elderly patients with cognitive impairment. Parkinsonian rigidity presents with lead-pipe resistance that remains constant throughout the range of motion, regardless of the speed of passive movement, often with superimposed cogwheeling resulting from an underlying tremor. Parkinson disease is typically accompanied by other cardinal motor features including resting tremor, bradykinesia, and postural instability.

In contrast, paratonia is uniquely associated with dementia, and demonstrates variable resistance that changes with the speed and direction of movement. Resistance increases when movements are performed more quickly and occurs in any direction. Unlike Parkinson disease, paratonia does not respond to levodopa therapy.6 The absence of cogwheeling, lack of clasp-knife phenomenon, and velocity-dependent directionally variable resistance are key distinguishing features that help clinicians differentiate paratonia from other forms of hypertonia. Prevalence rises with disease progression, from about 5% in mild cognitive impairment to 10% in early dementia, and up to 90% to 100% in end-stage disease.1,2 Risk factors include vascular dementia, severity of cognitive decline, and diabetes mellitus.9

Diagnosis of paratonia requires the presence of dementia; involuntary, variable resistance to passive movement in multiple directions without a clasp-knife phenomenon; and exclusion of parkinsonian rigidity and spasticity.10 The Paratonia Assessment Instrument is a validated 5- to 10-minute bedside assessment tool with strong interobserver reliability10 where the person examining the patient moves the patient’s limbs slowly then faster. Paratonia is assessed using 5 operational subcriteria: involuntary variable resistance to passive movement, the resistance to passive movement is in any direction, no clasp-knife phenomenon, the degree of resistance correlates with the speed of movement, and resistance must be felt in either 1 limb in 2 movement directions or in 2 different limbs.10

Because no validated or reproducible tool currently exists to quantify the severity of paratonia, clinicians often rely on adjacent measures such as goniometric joint angle assessment, the Pain Assessment in Advanced Dementia scale, visual analogue scale, or the Clinical Global Impression observer-rated scale.11 A fit-for-purpose, United States Food and Drug Administration–compliant Paratonia Burden Scale is currently being developed.12

Pharmacologic treatments for paratonia are currently ineffective; levodopa does not improve rigidity in paratonia.6 Forceful passive mobilization is contraindicated, as evidence shows it can worsen paratonia severity and raise caregiver burden, possibly through microinjury and reflexive resistance.5,7

Evidence-based, person-centred interventions include several nonpharmacologic strategies. Carefully placing cushions to support the head, arms, and legs, and between the knees can statistically significantly reduce upper limb tone and increase elbow mobility, with standard pillows being sufficient and no need for costly positioning systems. Effects are typically short-term (15 to 30 minutes) and require frequent adjustment to patient comfort and body position.13 Gentle, rhythmic, oscillating movements (harmonic techniques) administered by physiotherapists before daily care prioritize relaxation and proprioceptive input rather than forceful stretching. Evidence supports some benefits, including increased joint range of motion, pain reduction during care, decreased caregiver load, and smoother care delivery.13

Although currently used off-label for paratonia, botulinum toxin A (BoNT-A) represents a mechanistically sound and promising therapeutic option for people living with paratonia. Both paratonia and poststroke spasticity result from central nervous system (CNS) injury, and treatment with BoNT-A is an intervention for both conditions because BoNT-A acts peripherally at the neuromuscular junction, blocking acetylcholine release, thereby reducing excessive muscle contraction regardless of upstream CNS cause.14 Outcomes include increased range of motion, greater ease of hygiene, and improved comfort, with effects lasting approximately 3 months before the need for retreatment.15

An essential element of managing paratonia is regular medication review to identify and, where possible, discontinue agents known to worsen rigidity such as antipsychotics and dopamine antagonists.5,6 For patients with comorbid diabetes, optimal glycemic control may be preventive by reducing advanced glycation end product formation in muscle tissue.16 Encouraging physical activity and adaptive movement may further help to mitigate risk, although evidence is currently limited.4,16